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Conclusions This study demonstrate that prior HE, which caused a significant elevation of blood [lactate], resulted in an increased time to exhaustion during subsequent perimaximal exercise presumably by enabling a greater aerobic contribution to the energy requirement of exercise.

Gerbino et al. (14) demonstrated that the performance of heavy intensity exercise (i.e., exercise above the gas exchange threshold; GET), but not moderate-intensity exercise (<GET), speeded the overall pulmonary oxygen uptake (V̇O2) kinetics during subsequent heavy-intensity exercise. This speeding of the overall V̇O2 response was shown subsequently to result from a reduction in the amplitude of the V̇O2 “slow component” with no change in the time constant of the fundamental V̇O2 response in phase II (10,20). In studies in which sufficient time was allowed between exercise bouts to restore baseline V̇O2, prior heavy-intensity exercise resulted in an increased amplitude of the fundamental response and a reduction in the amplitude of the V̇O2 slow component with a similar end-exercise V̇O2 at 6–8 min (3,7,8). This altered V̇O2 response was associated with a reduction in the accumulation of blood [lactate] over the exercise bout, an attenuated V̇CO2 response, and a reduced overall O2 deficit. In keeping with these observations, measurements of muscle blood flow, arterial-femoral venous O2 difference, and the changes in and release of muscle metabolites indicate an increased oxidative contribution to energy metabolism and a reduction in substrate level phosphorylation in the second of two high-intensity exercise bouts with no change in total ATP turnover (1,23). A recent magnetic resonance spectroscopy study has confirmed that prior heavy-intensity exercise results in a significant sparing of intramuscular [PCr] during subsequent heavy intensity exercise (29).

There is consensus, therefore, that prior heavy-intensity exercise reduces the overall O2 deficit, limits the depletion of intramuscular [PCr] and the production of lactic acid, and attenuates the V̇O2 slow component during subsequent heavy exercise. These effects would be expected to increase exercise tolerance (14,17,28) or at least to allow a better tolerance of exercise than might be expected for the prevailing metabolic conditions (14). The purpose of this study was therefore to test the hypothesis that prior heavy-intensity exercise would extend the time to exhaustion during subsequent perimaximal exercise.

METHODS

Participants.

Seven healthy males (mean ± SD 27 ± 3 yr; 78.4 ± 0.7 kg) volunteered to participate in this study that was approved by the Manchester Metropolitan University ethics committee. All participants gave their written informed consent after the benefits and risks of participation in the study had been explained to them. The participants were regularly active in recreational exercise but were not highly trained.

Experimental design.

The participants visited the laboratory on seven occasions over a 3-wk period. The first visit was used to determine the V̇O2peak and GET, and the other visits were used to complete the experimentation. On a given day, participants exercised to exhaustion at either 100, 110, or 120% of the work rate at V̇O2peak (see below), after either no prior exercise (control condition) or after prior heavy-intensity exercise.

The experimental conditions were presented to the participants in a counterbalanced design. All participants reported to the laboratory rested (having performed no strenuous activity in the preceding 24-h), well hydrated, and having abstained from food, alcohol, and caffeine in the 3-h before testing. Tests were conducted in an air-conditioned laboratory (temperature 19°C) at the same time of day for each participant (± 2 h) and were separated by at least 24 h.

Measurement of GET and V̇O2peak.

All tests were performed on an electronically braked cycle ergometer (Ergoline, Jaeger), which controlled external work rate independent of pedal cadence. Participants self-selected a cadence for the V̇O2peak test (this ranged between 80 and 90 rpm). Although it is known that cadence can influence time to exhaustion, this was controlled for in the present study because all exercise tests were performed at the same cadence (± 2 rpm for any given subject). The V̇O2peak test began with 3 min of baseline cycling at 20 W (the lowest work rate available on the ergometer), after which work rate was increased by 30 W·min−1 until volitional exhaustion (reached in 9–11 min). Throughout the test, pulmonary gas exchange was measured breath-by-breath as described below. The V̇O2peak was determined as the highest value recorded in any 30-s period before the participant’s volitional termination of the test. The GET was determined as the first disproportionate increase in V̇CO2 from visual inspection of individual plots of V̇CO2 versus V̇O2 by an experienced reviewer. The work rate at V̇O2peak (W-V̇O2peak) was defined as the work rate at which V̇O2 began to plateau near the end of the test (N = 5) or reached its highest value when no plateau was evident (N = 2). For each individual, work rates equivalent to 50% Δ (half-way between the work rate at the gas exchange threshold (GET) and W-V̇O2peak; heavy-intensity exercise), and 100, 110, and 120% of the W-V̇O2peak (perimaximal exercise) were calculated.

Experimental tests.

Participants were required to maintain a low (100% W-V̇O2peak), medium (110% W-V̇O2peak), or high (120% W-V̇O2peak) perimaximal work rate for as long as possible. These exhaustive bouts were preceded either by no prior exercise (control condition) or by heavy-intensity prior exercise. The participants were not aware of the purpose of the study, and at no point during or after any test was information given regarding performance time.

The prior exercise conditions involved participants performing 3 min of baseline cycling at 20 W, followed by a square-wave transition to a work rate requiring 50% Δ; this work rate was maintained for 6 min. After the prior exercise bout, the participants rested for 7 min before cycling at 20 W for a further 3 min. The work rate was then increased abruptly to the predetermined perimaximal work rate (100, 110, or 120% of W-V̇O2peak), and participants attempted to maintain this work rate for as long as possible. The exhaustive trial was terminated when the self-selected cadence dropped by >5 rpm. Time to exhaustion was recorded to the nearest second. The perimaximal bouts performed in the control condition were identical except that they were not preceded by heavy-intensity exercise. Critical power (CP) and anaerobic work capacity (W ′) (28) were calculated from the three perimaximal exercise bouts performed in each condition using the linear model of work rate versus 1/time.

Fingertip blood samples (25 μL) were collected into a capillary tube immediately before and immediately after the perimaximal exercise bouts. Blood samples were subsequently analyzed for blood [lactate] using an automated lactate analyser (YSI stat 2300, Yellow Springs, OH). This analyzer was calibrated before each test with a 5-mM lactate standard supplied by the manufacturer (YSI 2747).

Measurement of pulmonary gas exchange and heart rate.

Pulmonary gas exchange was measured breath by breath during all exercise tests. Participants breathed through a low-resistance volume transducer (Jaeger Triple V, Hoechberg, Germany), which had a dead space of 90 mL. Gas was continuously drawn down a capillary line into rapid-response gas analyzers (Jaeger Oxycon Alpha). Gas exchange variables were calculated and displayed breath by breath once the delay between the volume and concentration signals had been accounted for. The volume transducer was calibrated before each test with a 3-L calibration syringe, and the analyzers were calibrated with gases of known concentration. Heart rate was recorded every 5-s by using short range telemetry (Polar PE 4000, Kempele, Finland).

Baseline V̇O2 was defined as the average of the V̇O2 values measured between the second and third minutes of exercise at 20 W before the transitions to the perimaximal work rates. The V̇O2 at 1 min of the exhaustive bouts was calculated from the average V̇O2 of a 30-s period centred on 1 min. The end V̇O2 was defined as the average of the V̇O2 values measured during the last 30 s of exercise. The response curves of V̇O2 were also described using mathematical modeling procedures. The V̇O2 response to supra-maximal exercise (110 and 120% W-V̇O2peak) was expected to conform to a mono-exponential function after the cardiodynamic phase, whereas the response to exercise at 100% W-V̇O2peak might have been complicated by the emergence of the V̇O2 slow component (26). To allow a comparison of the rate of V̇O2 response after the onset of exercise, the data were modeled using both single and double exponential models in order to isolate the V̇O2 fast component response. The initial cardiodynamic component was ignored by eliminating the first 20 s of data after the onset of exercise. The models used can be expressed as follows:EQUATIONEQUATION

The exponential models included amplitudes (Ap and As), time constants (τp and τs), and delay times (Tdp and Tds). Ap, τp, and Tdp describe the V̇O2 fundamental component, while As, τs, and Tds describe the V̇O2 slow component. A nonlinear least-square algorithm was used to determine the parameters of the best fitting curve. The mean-square amplitudes were used to evaluate whether the monoexponential or biexponential model provided the best fit to each data set. Owing to concerns over the relatively low signal/noise ratio with only one exercise transition in each condition, we chose to report only the mean response time for the primary phase of the response (TDp + τp).

Statistical analysis.

Differences in time to exhaustion and physiological response between the perimaximal exercise bouts preceded by no prior exercise and those preceded by heavy-intensity prior exercise were tested for statistical significance using paired t-tests. Statistical significance was set at P < 0.05.

RESULTS

The mean (± SD) V̇O2peak of the participants was 50.3 ± 3.3 mL·kg−1·min−1, with GET occurring at 52 ± 12% of V̇O2peak. Heavy-intensity prior exercise was performed at 253 ± 51 W (N = 7). The work rates used in the exhaustive bouts were 322 ± 39, 357 ± 43, and 392 ± 48 W for the 100, 110, and 120% W-V̇O2peak conditions, respectively.

Time to exhaustion was significantly longer in all of the perimaximal bouts after heavy-intensity prior exercise compared with the control condition (Table 1 and Fig. 1). The CPwas not significantly affected by the performance of prior high-intensity exercise (control: 284 ± 35 vs heavy exercise: 289 ± 26 W), but the increase in W′ approached statistical significance (control: 15.5 ± 2.2 vs heavy exercise: 18.2 ± 3.5 kJ; P = 0.06), (Fig. 2). Heavy-intensity prior exercise caused a significant increase in blood [lactate], which was still present at the onset of the perimaximal exercise bouts (Table 1). However, no significant differences in blood [lactate] were observed at the termination of the perimaximal exercise bouts. Heart rate immediately before the onset of the perimaximal exercise bouts was significantly higher after prior heavy-intensity exercise compared with control (Table 1). This higher heart rate persisted throughout exercise and was still evident at the cessation of the exhaustive bouts, reaching significance at 110% and 120% W-V̇O2peak (P < 0.05).

Table 2 shows the V̇O2 responses to perimaximal exercise after no prior exercise and after heavy-intensity prior exercise. There was no significant difference in baseline V̇O2 at the onset of the perimaximal exercise bouts between the control and prior heavy-intensity exercise conditions. The V̇O2 kinetics in the primary adaptive phase (as given by the mean response time) were not significantly altered by the performance of prior heavy-intensity exercise. At 100% W-V̇O2peak, there was no significant difference in the V̇O2 at 1 min into exercise or at exhaustion. At 110% W-V̇O2peak, V̇O2 at 1 min into exercise was significantly higher than in the control condition (P < 0.05), but there was no significant difference in the V̇O2 at exhaustion. At 120% W-V̇O2peak, V̇O2 was significantly higher both at 1 min into exercise (P < 0.05) and at exhaustion (P < 0.05) compared with the control condition.

DISCUSSION

Consistent with our hypothesis, the results indicate that prior heavy-intensity exercise leads to a significant increase in time to exhaustion during subsequent perimaximal exercise. Previous research has demonstrated that prior high-intensity exercise results in an increased oxidative contribution to energy metabolism during subsequent high-intensity exercise, with a corresponding reduction in the oxygen deficit, as reflected in a reduced rate of substrate-level phosphorylation (1,6,23,24,29). There is direct evidence that muscle blood flow and O2 extraction are increased during high-intensity cycle exercise when it is preceded by a high-intensity warm-up (1,23). Furthermore, Rossiter et al. (29) reported that prior heavy leg extension exercise resulted in a 9% sparing of [PCr] over the first 2–3 min of an identical exercise bout performed 6 min later. Other groups have also shown that total anaerobic energy turnover is substantially reduced (by 25–45%) in the second of two high-intensity exercise bouts (1,11,23). The reduced lactate production and sparing of intramuscular [PCr] resulting from the increased muscle aerobic energy turnover might be expected to predispose to increased exercise tolerance (14), as indeed we found in the present study. This is because the point of exhaustion is often presumed to coincide with a depletion of intra-muscular phosphates to some critical value and/or the attainment of a critically low intracellular pH or high [lactate] (but see below) (12,15,27,28).

In the present study, the performance of prior heavy-intensity exercise led to a dramatic increase in the time to exhaustion during subsequent perimaximal exercise (29–59% compared with the control condition). Interestingly, however, prior heavy-intensity exercise did not cause a significant improvement in the CP but did influence the curvature constant of the power-time relationship, resulting in an increased W′ that approached statistical significance. It is likely that the difference in W′ would have reached statistical significance if our subject sample had been slightly larger, indicating that this is a real effect that is worthy of further investigation. The W′ is considered to represent a finite energy reserve comprising O2 stores (note that this would be relatively small), high-energy phosphates, and energy derived through anaerobic glycolysis (28). It is unclear, therefore, how the performance of heavy exercise might enhance the derivation of energy through predominantly O2-independent pathways (i.e., increase the “anaerobic capacity”) unless the effect of prior heavy-intensity exercise is to retard the rate at which metabolites that ultimately result in fatigue accumulate during subsequent exercise (see below).

It is important to point out that the performance of prior moderate-intensity exercise (i.e., “warm-up”) does not alter the V̇O2 or blood [lactate] response to subsequent exercise (10,14). Furthermore, moderate-intensity warm-up exercise does not appear to enhance performance during subsequent high-intensity endurance exercise (5,21). We have recently found that 12 min of prior moderate-intensity exercise, that would have resulted in a similar total energy expenditure to the prior heavy-intensity exercise bout performed in the present study, had a relatively small effect (+2–5%) on the time to exhaustion in subsequent perimaximal exercise bouts (Jones et al., unpublished observations, 2003). It has also been demonstrated that the elevation of muscle temperature by 2–3°C using hot packs or water baths (9,19,22) does not appreciably alter the V̇O2 or blood [lactate] response to subsequent exercise. Collectively, these results suggest that the extended time to exhaustion in the perimaximal bouts after prior heavy-intensity exercise was unlikely to be contingent on an increased muscle temperature.

Blood [lactate] was significantly elevated at the onset of the perimaximal exercise trials after prior heavy-intensity exercise (2.5 mM), and it might appear paradoxical that time to exhaustion was extended in the face of this residual acidosis. Both the lactate ion and the hydrogen ion have been shown to reduce force production in isolated muscle (15,27), and the accumulation of lactate and the reduction of pH during heavy exercise in humans is believed by many to be a major cause of muscle fatigue (13). However, many of the early studies that led to this view were conducted at unphysiologically low temperatures (17°C), and when these experiments are repeated at 37°C, the inhibitory effect of intracellular acidification on muscle contractility disappears (30). In an important recent study, Nielsen et al. (25) reported that the addition of 20-mM lactic acid to an isolated muscle preparation almost completely reversed the 75% loss of tetanic force caused by preincubation at an extra-cellular [K+] of 11 mM. These data indicate that, rather than causing fatigue, acidosis might protect against fatigue resulting from the loss of muscle K+ during exercise, at least in some situations. In the present study, it is therefore possible that the residual acidosis after prior heavy-intensity exercise served to preserve muscle function and retard the rate at which fatigue developed during the subsequent high-intensity exercise bouts.

It appears that the extent of the metabolic acidosis caused by prior exercise is important in determining the potential for performance enhancement (2,16,18). For example, Karlsson et al. (18) reported that prior exhaustive arm exercise that increased blood [lactate] to 10 mM resulted in a 31% reduction in the time to exhaustion in exhaustive leg cycle exercise performed 6 min later. More recently, Koppo and Bouckaert (21) reported that prior exercise at 90% V̇O2peak (as compared with 75% V̇O2peak in the present study), which resulted in a blood [lactate] of 6 mM, did not significantly alter time to exhaustion during subsequent exercise at 95% V̇O2peak. Also, Bishop et al. (5) reported that a continuous heavy-intensity warm-up at 75% V̇O2peak, which elevated blood [lactate] to 5.1 mM, did not improve performance in a 2-min all-out kayak ergometer test. It is possible that very-high-intensity prior exercise results in the accumulation of other fatiguing metabolites (e.g., Pi, H2PO4−, ammonia) in muscle (30), or that more time is subsequently required for the restoration of extracellular [K+] (2). Therefore, differences in the rate of lactate clearance compared with the rate of clearance of other “fatiguing” metabolites and the speed with which the electrochemical gradient across the muscle membrane is restored may be important in determining the potential for performance enhancement. It may be that there is an optimal blood [lactate] of 2–3 mM that is required for performance enhancement because prior exercise that either results in no change in blood [lactate], or prior exercise and recovery combinations that result in large elevations in blood [lactate] of greater than 5 mM, does not enhance performance (5,18,21). Moderate-intensity warm-up exercise does not enhance the aerobic contribution to subsequent exercise (10,14), whereas severe-intensity warm-up exercise may not allow sufficient time for restoration of intramuscular high-energy phosphates and/or removal of fatiguing metabolites (e.g., Pi,H+, H2PO4−, or extra-cellular K+) before the commencement of the criterion exercise challenge.

Although somewhat controversial, it appears that priming exercise does not result in a speeding of the V̇O2 kinetics over the primary adaptive phase of the response during subsequent cycle exercise but that V̇O2 projects to a greater initial amplitude with an unchanged time constant (3,7,8). In the present study, the overall primary V̇O2 kinetics expressed as the mean response time were not significantly affected by prior exercise; rather, V̇O2 appeared to project to and/or reach a higher V̇O2 in the perimaximal exercise bouts with a similar rate of response. Indeed, at 120% W-V̇O2peak, the increased time to exhaustion resulting from the performance of prior heavy-intensity exercise allowed V̇O2peak to be attained, whereas in the control condition exercise was terminated before V̇O2peak was reached (Fig. 3). As mentioned above, this suggests that the mechanism(s) causing fatigue in the control condition were in some way attenuated by the performance of prior high-intensity exercise.

The mechanisms responsible for the elevated V̇O2 throughout the transient phase of heavy exercise when it is preceded by a bout of heavy exercise are still debated, but these might feasibly include changes in O2 availability, enzyme activity, substrate availability, or motor unit recruitment (4,7,11,14). Gerbino et al. (14) suggested that the residual acidosis after a priming bout of heavy exercise might increase muscle vasodilation and result in more homogeneous muscle perfusion at exercise onset. For perimaximal exercise, at least, reduction of any heterogeneity in oxygen delivery to working muscle would be expected to increase V̇O2 and diminish Δ [lactate]. Alternatively, it is possible that changes in putative controllers of muscle respiration such as the phosphorylation potential, [PCr], NADH availability, and cytosolic [Ca2+] after prior heavy exercise might reduce any inherent inertia in the key enzymes controlling oxidative metabolism and result in either a reduced “lag” before muscle O2 consumption increases appreciably after the onset of subsequent exercise (4) or a more rapid adjustment to the “steady state” requirement. It is also known that prior exercise results in a stockpiling of acetyl groups, and it has been suggested that this greater availability of metabolic substrate might enhance mitochondrial ATP production (11). Finally, it has been suggested that the increased V̇O2 might be related to increased motor unit recruitment at the onset of exercise. Burnley et al. (7) reported that muscle iEMG was 19% higher at the onset of the second of two bouts of severe-intensity exercise and noted that the iEMG responses were qualitatively similar to the pulmonary V̇O2 responses in both bouts. Increased motor unit recruitment at the onset of heavy constant work rate exercise might be beneficial to performance because the metabolic strain on each fiber would be reduced.

In conclusion, the performance of prior high-intensity exercise resulted in a significant increase in time to exhaustion during subsequent perimaximal exercise at 100%, 110%, and 120% W-V̇O2peak despite, or perhaps because of, a significant elevation of blood [lactate] (to 2.5 mM) at exercise onset. The results of this study may have important implications for the preparation of athletes for competition and for the improvement of exercise tolerance in the elderly and in patient populations. The characteristics of the prior exercise intensity, exercise duration, exercise mode, and recovery period that optimize the ergogenic effect of prior heavy-intensity exercise remain to be determined. Elucidation of these characteristics, and examination of the effect of prior heavy-intensity exercise on performance both in athletes and in populations with compromised exercise tolerance, may be fruitful topics for future research.